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IntroductionThe precise pathophysiology of common atrial flutter remains imperfectly known. The mechanisms of arrhythmia initiation and the role of areas of slow conducting myocardium and functional block are still debated topics.MethodsWe conducted a detailed electrophysiological study of a patient to illustrate and refine these concepts. Prior to CTI ablation, electrophysiological study and electro-anatomical mapping were performed, focusing on initiation and maintenance mechanisms of the arrhythmia.ResultsThe initiation of common atrial flutter takes place on the septal aspect of the cavo-tricuspid isthmus where functional unidirectional conduction block occurs. The direction of activation is therefore frequently counter-clockwise, and the arrhythmia stabilizes around the vena cavas and sinus venosus/crista terminalis region. No conduction slowing is present.ConclusionsCommon atrial flutter initiates when functional unidirectional conduction block occurs on the septal cavotricuspid isthmus. Its rotation is limited by anatomical and functional boundaries.

An early repolarization pattern can be observed in 1% up to 13% of the overall population. Whereas, this pattern was associated with a benign outcome for many years, several more recent studies demonstrated an association between early repolarization and sudden cardiac death, so-called early repolarization syndrome. In early repolarization syndrome patients, current imbalances between epi- and endo-cardial layers result in dispersion of de- and repolarization. As a consequence, J waves or ST segment elevations can be observed on these patients' surface ECGs as manifestations of those current imbalances. Whereas, an early repolarization pattern is relatively frequently found on surface ECGs in the overall population, the majority of individuals presenting with an early repolarization pattern will remain asymptomatic and the isolated presence of an early repolarization pattern does not require further intervention. The mismatch between frequently found early repolarization patterns in the overall population, low incidences of sudden cardiac deaths related to early repolarization syndrome, but fatal, grave consequences in affected patients remains a clinical challenge. More precise tools for risk stratification and identification of this minority of patients, who will experience events, remain a clinical need. This review summarizes the epidemiologic, pathophysiologic and diagnostic background and presents therapeutic options of early repolarization syndrome.

AF is a heterogeneous rhythm disorder that is related to a wide spectrum of etiologies and has broad clinical presentations. Mechanisms underlying AF are complex and remain incompletely understood despite extensive research. They associate interactions between triggers, substrate and modulators including ionic and anatomic remodeling, genetic predisposition and neuro-humoral contributors. The pulmonary veins play a key role in the pathogenesis of AF and their isolation is associated to high rates of AF freedom in patients with paroxysmal AF. However, ablation of persistent AF remains less effective, mainly limited by the difficulty to identify the sources sustaining AF. Many theories were advanced to explain the perpetuation of this form of AF, ranging from a single localized focal and reentrant source to diffuse bi-atrial multiple wavelets. Translating these mechanisms to the clinical practice remains challenging and limited by the spatio-temporal resolution of the mapping techniques. AF is driven by focal or reentrant activities that are initially clustered in a relatively limited atrial surface then disseminate everywhere in both atria. Evidence for structural remodeling, mainly represented by atrial fibrosis suggests that reentrant activities using anatomical substrate are the key mechanism sustaining AF. These reentries can be endocardial, epicardial, and intramural which makes them less accessible for mapping and for ablation. Subsequently, early interventions before irreversible remodeling are of major importance. Circumferential pulmonary vein isolation remains the cornerstone of the treatment of AF, regardless of the AF form and of the AF duration. No ablation strategy consistently demonstrated superiority to pulmonary vein isolation in preventing long term recurrences of atrial arrhythmias. Further research that allows accurate identification of the mechanisms underlying AF and efficient ablation should improve the results of PsAF ablation.

Idiopathic ventricular fibrillation (IVF) is the main cause of unexplained sudden cardiac death, particularly in young patients under the age of 35. IVF is a diagnosis of exclusion in patients who have survived a VF episode without any identifiable structural or metabolic causes despite extensive diagnostic testing. Genetic testing allows identification of a likely causative mutation in up to 27% of unexplained sudden deaths in children and young adults. In the majority of cases, VF is triggered by PVCs that originate from the Purkinje network. Ablation of VF triggers in this setting is associated with high rates of acute success and long-term freedom from VF recurrence. Recent studies demonstrate that a significant subset of IVF defined by negative comprehensive investigations, demonstrate in fact subclinical structural alterations. These localized myocardial alterations are identified by high density electrogram mapping, are of small size and are mainly located in the epicardium. As reentrant VF drivers are often colocated with regions of abnormal electrograms, this localized substrate can be shown to be mechanistically linked with VF. Such areas may represent an important target for ablation.